NF-κB (核因子κB)

Nuclear factor-κB; Nuclear factor-kappaB

NF-κB (Nuclear factor kappa-light-chain-enhancer of activated B cells) is a protein complex that controls transcription of DNA. NF-κB is found in almost all animal cell types and is involved in cellular responses to stimuli such as stress, cytokines, free radicals, ultraviolet irradiation, oxidized LDL, and bacterial or viral antigens. NF-κB plays a key role in regulating the immune response to infection. Incorrect regulation of NF-κB has been linked to cancer, inflammatory, and autoimmune diseases, septic shock, viral infection, and improper immune development. NF-κB has also been implicated in processes of synaptic plasticity and memory. There are five proteins in the mammalian NF-κB family: NF-κB1, NF-κB2, RelA, RelB, c-Rel.

NF-κB 亚型特异性产品:

NF-κB Isoform Comparison

NF-κB 相关产品 (727)
抗体 (30)
NF-κB 信号通路
NF-κB Isoform Comparison

By Effects:	抑制剂 (613) 激动剂 (5) 降解剂 (1) 激活剂 (27) 调节剂 (17) 诱导剂 (2)

Cat. No.	Product Name	Effect	Purity	Chemical Structure

HY-18935A

CBL0137 hydrochloride	Inhibitor	99.66%
CBL0137 hydrochloride 是组蛋白分子伴侣 FACT 的抑制剂。CBL0137 hydrochlorideye 也可以激活 p53 并抑制 NF-κB，对于它们的 EC₅₀ 值分别为 0.37 和 0.47 μM。

HY-N0191

Andrographolide 穿心莲内酯	Inhibitor	99.89%
Andrographolide 是一种 NF-κB 抑制剂，通过共价修饰内皮细胞中 p50 的半胱氨酸残基而抑制 NF-κB 活化，而不影响 IκBα 降解或 p50/p65 核易位。Andrographolide 具有抗病毒作用。

HY-19356

Rocaglamide 楝酰胺	Inhibitor	99.34%
Rocaglamide (Roc-A) 是从楝科植物中分离出来，可用于咳嗽，受伤，哮喘和炎症性皮肤病。Rocaglamide 是 T 细胞中一种有效的 NF-κB 活化抑制剂。Rocaglamide 是一种有效的选择性热休克因子 1 (HSF1) 活化抑制剂，IC₅₀ 约为 50 nM。Rocaglamide 还抑制翻译起始因子 eIF4A 的功能。Rocaglamide 还具有抗癌特性。

HY-10257

BAY 11-7085	Inhibitor	99.99%
BAY 11-7085 (BAY 11-7083) 是 NF-κB 激活和 IκBα 磷酸化的抑制剂，稳定 IκBα 的 IC₅₀ 值为 10 μM。

HY-P1956

Human serum albumin	Inhibitor	99.9%
Human serum albumin (HSA) 是血浆中含量最高的蛋白质，是影响血浆瘤压的主要因素。Human serum albumin 具有抗氧化、抗凝血、抗炎、抗血小板聚集活性以及胶体渗透作用。Human serum albumin 能阻止 GML 抑制人类 T 细胞的能力，实现对 T 细胞功能的保护。Human serum albumin 也与心血管疾病相关，能部分阻止 LPS (HY-D1056) 诱导的氧化应激以及血管壁中 NF-κB、iNOS 和过氧亚硝酸根 (ONOO⁻) 上调的血压降低。

HY-B2163

Astaxanthin 虾青素	Inhibitor	≥98.0%
Astaxanthin，红色膳食类胡萝卜素，是一种口服有效的强效抗氧化剂。Astaxanthin 可抑制 NF-κB，能在蛋白质水平下调高血糖中的 VEGF。Astaxanthin 通过激活 PPARγ 并减少 STAT3 和相关通路蛋白的表达，发挥抗癌细胞增殖、增加凋亡以及削弱迁移和侵袭的活性。Astaxanthin 还具有神经保护和抗炎活性可用于癌症，糖尿病视网膜病变，心血管疾病等研究以及动物饲料的着色。

HY-10529

Betulinic acid 白桦脂酸	Modulator	98.43%
Betulinic acid 是一种天然的五环三萜类化合物，为真核细胞拓扑异构酶 I (topoisomerase I) 的抑制剂，IC₅₀ 值为 5 μM，具有抗炎，抗疟疾，抗艾滋病和抗肿瘤等活性。

HY-10496

SC75741	Inhibitor	99.51%
SC75741 是一种广泛，有效的 NF-κB 抑制剂，对 p65 的 IC₅₀ 为 200 nM。SC75741 可阻断 influenza viruses 复制。SC75741 通过损害 NF-κB 亚基 p65 的 DNA 结合，导致细胞因子，趋化因子和促凋亡因子的表达降低，抑制 caspase 活化和阻断 caspase 介导的病毒核糖核蛋白 (viralribonucleoproteins) 的核输出。

HY-N0603

20(S)-Ginsenoside Rg3 20(S)-人参皂苷 Rg3	Inhibitor	99.94%
20(S)-Ginsenoside Rg3 是人参的主要成分。20(S)-Ginsenoside Rg3 抑制 Na⁺ 和 hKv1.4 通道，IC₅₀ 分别为 32.2±4.5 和 32.6±2.2 μM。20(S)-Ginsenoside Rg3 还抑制 Aβ，NF-κB 活性和 COX-2 表达。

HY-N0039

Ginsenoside Rb1 人参皂苷 Rb1	Inhibitor	98.75%
Ginsenoside Rb1 是中药人参的成分。Ginsenoside 抑制 Na⁺, K⁺-ATPase 活性，IC₅₀ 为 6.3±1.0 μM。Ginsenoside Rb1 也抑制 IRAK-1 激活及 NF-κB p65 的磷酸化。

HY-N0045

Ginsenoside Rg1 人参皂苷 Rg1	Inhibitor	99.91%
Ginsenoside Rg1 是人参的主要活性成分之一。Ginsenoside Rg1 改善认知功能受损，通过降低大脑 Aβ 水平来发挥作用。Ginsenoside Rg1 减少 NF-κB 核易位。

HY-134476

NF-κΒ activator 1	Activator	99.94%
NF-κΒ activator 1 (compound 32) 是一种有效的 NF-κΒ 激活剂，EC₅₀ 为 0.9 μM，NF-κΒ activator 1 诱导超氧化物歧化酶 (SOD)2 mRNA表达。

HY-B0190A

Nafamostat mesylate 甲磺酸萘莫司他		99.85%
Nafamostat mesylate (FUT-175)，一种抗凝剂，是一种人工合成的丝氨酸蛋白酶 (serine protease) 抑制剂。 Nafamostat mesylate 具有抗癌和抗病毒作用，Nafamostat mesylate 通过上调肿瘤坏死因子受体 1 (TNFR1) 的表达诱导凋亡 (apoptosis)，可用于动脉壁病理性增厚的发生发展。

HY-N2065

Withaferin A 醉茄素A	Inhibitor	99.92%
Withaferin A 是从睡茄中分离到的甾体内酯，可以抑制 NF-kB 的活性，靶作用于波形蛋白 (vimentin)，具有抗炎，抗肿瘤等功效。Withaferin A 是内皮蛋白 C 受体 (EPCR) 脱落的抑制剂。

HY-13812

QNZ	Inhibitor	99.50%
QNZ (EVP4593) 强抑制 NF-κB 转录激活和 TNF-α 产生，IC₅₀ 分别为 11 和 7 nM。QNZ (EVP4593) 是一种保护神经的钙池操纵的钙通道 (SOC) 抑制剂。

HY-P0151

SN50	Inhibitor	99.98%
SN50是可渗透细胞的 NF-κB 易位抑制剂。

HY-123942

Diprovocim	Agonist	98.35%
Diprovocim 是一种有效的 TLR1/TLR2 激动剂。Diprovocim 在人 THP-1 细胞中引发完全激动剂活性 (EC₅₀=110 pM)。Diprovocim 刺激小鼠巨噬细胞释放 TNF-α (EC₅₀=1.3 nM)。Diprovocim 激活下游 MAPK 和 NF-κB 信号通路。Diprovocim 在小鼠中显示出很强的佐剂活性，尤其是促进细胞免疫反应。

HY-N0452

Hyperoside 金丝桃甙	Inhibitor	99.50%
Hyperoside 是一种 NF-κB 抑制剂，从 Hypericum monogynum 中发现。Hyperoside 具有抗肿瘤、抗真菌、抗炎症、抗病毒和抗氧化的活性，并能诱导细胞凋亡。

HY-N1445

Isoquercitrin 异槲皮苷	Inhibitor	99.87%
Isoquercetin (Quercetin 3-glucoside) 是天然存在的多酚，具有抗氧化，抗增殖和抗炎特性。Isoquercetin 通过 Nrf2/ARE 抗氧化剂信号传导途径减轻乙醇诱导的肝毒性，氧化应激和炎症反应。Isoquercetin 通过调节核因子-κB (NF-κB) 转录调节系统调节一氧化氮合酶 2 (NO2) 的表达。Isoquercetin 具有高生物利用度和低毒性，是预防糖尿病妊娠出生缺陷的有希望的候选活性分子。

HY-P1860

TNF-α (31-45), human	Activator	99.77%
TNF-α (31-45), human 是一种有效的 NF-kB 通路激活剂，也是一种促炎细胞因子，可诱导坏死或凋亡。TNF α 通过 TNFR2 刺激 NF-κB 通路，促进癌症生长、侵袭和转移。

LAT TCR CD3 BCR PLCγ1 ZAP70 PKC ELKs NEMO ATM NEMO PIASy PIDD RIP1 PARP1 NEMO ATM cIAP1 NEMO ATM c-IAP1/2, c-FLIP, XIAP, Bcl-XL, Bcl-2, gadd45β,
TRAF1/2, A1/Bfl-1, p100, IL-1, IL-6, IL8, IL-1β, TNF-α, A20,
IκBα, COX2, MIP-1β, MIP-2, VCAM-1,GM-CSF, CCL2, etc. IκBα TRAF6 ATM Tyr kinase LYN SYK BLK BLNK PLCγ2 BTK CARMA1 MALT1 BCL-10 IκBα CK2 p50 RELA IL-1 IL-1R MyD88 IRAK1 IRAK4 TRAF6 TNF TNFR1 TRADD RIPK1 TRAF2/5 cIAP1/2 TAB2 or
TAB3 TAK1 NEMO IKKα IKKβ p105 p50 p105 REL p50 p50 p50 REL p50 RELA p50 c-REL p50 p50 IκBα REL p50 REL p50 CREB TRIM25 RNF135 IPS1 TRAF3 TRAF2/6 Virus MKK3 or
MKK6 MKK4 or
MKK7 p38 JNK CREB AP1 AP1 LPS LBP CD14 TLR4 MD2 MD2 MD2 TLR4 MyD88 TIRAP TRAM TRIF IRAK1 IRAK4 TRAF6 RIP1 TRAF3 CD40L, RANKL CD40,
RANK LTα1β2, LIGHT,
BAFF LTβR,
BAFFR TRAF6 IKKε TBK1 IRF7 IRF3 IRF3 IRF7 BLC, ELC, SLC, SDF-1α, BAFF,
ICAM, CXCL12, CXCL13, CCL19, CCL21, etc. TRAF3 TRAF2 cIAP1/2 NIK TBK1 IKKα p100 RELB p52 RELB p52 RELB

Download NF-κB Signaling Pathway Map.

NF-κB transcription factors are critical regulators of immunity, stress responses, apoptosis and differentiation. In mammals, there are five members of the transcription factor NF-κB family: RELA (p65), RELB and c-REL, and the precursor proteins NF-κB1 (p105) and NF-κB2 (p100), which are processed into p50 and p52, respectively. NF-κB transcription factors bind as dimers to κB sites in promoters and enhancers of a variety of genes and induce or repress transcription. NF-κB activation occurs via two major signaling pathways: the canonical and the non-canonical NF-κB signaling pathways^[1].

The canonical NF-κB pathway is triggered by signals from a large variety of immune receptors, such as TNFR, TLR, and IL-1R, which activate TAK1. TAK1 then activates IκB kinase (IKK) complex, composed of catalytic (IKKα and IKKβ) and regulatory (NEMO) subunits, via phosphorylation of IKKβ. Upon stimulation, the IKK complex, largely through IKKβ, phosphorylates members of the inhibitor of κB (IκB) family, such as IκBα and the IκB-like molecule p105, which sequester NF-κB members in the cytoplasm. IκBα associates with dimers of p50 and members of the REL family (RELA or c-REL), whereas p105 associates with p50 or REL (RELA or c-REL). Upon phosphorylation by IKK, IκBα and p105 are degradated in the proteasome, resulting in the nuclear translocation of canonical NF-κB family members, which bind to specific DNA elements, in the form of various dimeric complexes, including RELA-p50, c-REL-p50, and p50-p50. Atypical, IKK-independent pathways of NF-κB induction also provide mechanisms to integrate parallel signaling pathways to increase NF-κB activity, such as hypoxia, UV and genotoxic stress.

The non-canonical NF-κB pathway is induced by certain TNF superfamily members, such as CD40L, BAFF and lymphotoxin-β (LT-β), which stimulates the recruitment of TRAF2, TRAF3, cIAP1/2 to the receptor complex. Activated cIAP mediates K48 ubiquitylation and proteasomal degradation of TRAF3, resulting in stabilization and accumulation of the NFκB-inducing kinase (NIK). NIK phosphorylates and activates IKKα, which in turn phosphorylates p100, triggering p100 processing, and leading to the generation of p52 and the nuclear translocation of p52 and RELB^[2][3].

Reference:

[1]. Oeckinghaus A, et al. The NF-kappaB family of transcription factors and its regulation.Cold Spring Harb Perspect Biol. 2009 Oct;1(4):a000034.
[2]. Taniguchi K, et al. NF-κB, inflammation, immunity and cancer: coming of age. Nat Rev Immunol. 2018 May;18(5):309-324.
[3]. Perkins ND,et al. Integrating cell-signalling pathways with NF-kappaB and IKK function. Nat Rev Mol Cell Biol. 2007 Jan;8(1):49-62.

NF-κB Isoform Comparison

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